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Medical Screening II > Lecture 2 > Flashcards

Lecture 2 Flashcards

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USMLE® Step 1 flashcards
1
Q

Physiology of Pain

A
  • Nociceptive: produced by injury
  • Neuropathic: nerve involvement
  • Psychogenic: origin of psychological nature
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2
Q

Opioid Analgesics

A
  • Alter pain perception
  • Used in moderate to severe pain
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3
Q

Opioid Analgesics are indicated in?

A
  • Acute pain
  • Chronic Pain
  • Antitussive (codeine in cough medicine)
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4
Q

Endogenous opioids

A
  • influence behavior (addiction)
  • control pain and inflammation
  • example: Endorphins
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5
Q

Opioid Receptors

A
  • Mu: mediating analgesia effect, most important
  • Kappa: Psychotic effects
  • Delta: Increase hormonal release; inhibits neurotransmitter release
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6
Q

Classification of opioids

A
  • Strong agonists: severe pain
  • Moderate agonists: moderate pain, antitussive
  • Mixed Agonists/ Antagonists: decreased risk of fatal overdose, fewer addictive qualities
  • Antagonists: help with overdoses, chronic pain
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7
Q

Metabolic inactivation of drugs takes place primarily in?

A
  • the liver
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8
Q

Opioid Mechanisms of Action can occur at which 3 different levels?

A
  • Spinal Cord level
  • Supraspinal Level
  • Peripheral Effects
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9
Q

Opioids act at the spinal cord level

A
  • inhibit painful impulses being sent from the peripheral to the brain
  • Bind to presynaptic nerve terminals: block synaptic transmission
  • Bind to postsynaptic terminals: block neurotransmitter, Decrease excitability of postsynaptic neuron
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10
Q

Opioid at Supraspinal Level

A
  • identified in the brain associated with pain transmission
  • exert analgesic effect by binding to supraspinal receptors
    -* Activating the descending pathways
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11
Q

Opioid at peripheral

A
  • receptors exist outside the CNS
  • peripheral ends of primary afferent (sensory) neurons
  • creating analgesic effect by decreasing the excitability of sensory neurons
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12
Q

Opioids: Clinical applications

A
  • moderate to severe pain
  • acute pain following surgery
  • cancer related chronic pain
  • maintain plasma concentrations
  • with anesthesia
  • Pulmonary edema to improve sense of ability to breathe
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12
Q

Adverse effects of Opioids

A
  • Sedation
  • Mood changes
  • Confusion
  • Respiratory Depression
  • Orthostatic hypotension
  • Nausea / vomiting
  • Constipation
  • Tolerance / Dependence
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13
Q

Special Concerns of Opioids for rehab patients

A
  • Sedation & GI discomfort
  • Timing of peak analgesic effect during rehab sessions
  • Respiratory response to exercise
  • Opioid-induced constipation
    -Withdrawal
  • Methadone (helps people to get off medication without too much withdrawal)
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14
Q

Opioid Induced hyperalgesia

A
  • Pain may worsen when drug is taking peak effect
  • Pain may improve when drug effects are minimal
  • Pain may improve when dosage is reduced
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15
Q

Prostaglandins (NSAIDS)

A
  • trauma / disturbances in homeostasis increase prostaglandin production
  • protective when it comes to responding to cellular injury
  • Mediate painful effects of injury and other effects of pathology
16
Q

Prostaglandins effect

A
  • Increase inflammatory response
  • Increase sensitivity of pain receptors
  • Fever
  • Dysmenorrhea ( affect menstrual cramps)
  • Thrombus formation (blood clot)
17
Q

Primary effects of NSAIDS

A
  • Analgesic
  • Anti-inflammatory
  • Antipyretic (for fever)
  • Anticoagulant
  • Possibly anticancer
18
Q

Reye’s syndrome

A
  • may be triggered by Asprin
  • Children and teenagers
  • Following the flu or chickenpox
  • High Fever
  • Vomiting
  • Liver dysfunction
  • Unresponsiveness / delirium
  • Death
19
Q

COX Enzyme

A
  • first step in the synthesis of prostaglandins and thromboxane
  • Involved in producing pain, inflammation, fever and clotting
20
Q

What is the key site of NSAID action within the cell

A

COX

21
Q

COX 1

A

regulate normal cell activity

22
Q

COX 2

A

produced primarily in injured cells

23
Q

Best clinical effects are achieved by?

A
  • inhibiting harmful prostaglandins from COX 2 while sparing production of COX 1
24
Q

NSAIDS: mechanism of action

A
  • inhibit synthesis of prostaglandins
  • Inhibit COX 2
25
Q

What is the potent inhibitor of COX enzymes

A
  • Aspirin (NSAID)
26
Q

Aspirin - clinical applications

A
  • treatment of pain and inflammation
  • treatment of fever
  • treatment of vascular disorders
  • Prevention of Cancer
27
Q

what is the primary problem with all NSAIDS?

A

gut tissue damage

28
Q

Susceptible patient populations of Adverse effects of aspirin like drugs

A
  • Advanced age
  • History of ulcers
  • Used of multiple NSAIDs
  • High doses of NSAIDs
  • use of anti-inflammatory steroids or anticoagulants
29
Q

Adverse effects of aspirin like drugs

A
  • inhibit platelet activity
  • increase blood pressure (inhibit vasoactive substances)
  • less vascular tone, increased bp, chance of MI or stroke
30
Q

COX 2 Selective Drugs

A
  • inhibit synthesis of prostaglandins in pain and inflammation
  • Spare production of beneficial prostaglandins in the stomach, kidneys and platelets
  • Decrease pain and inflammation with less toxicity
31
Q

COX 2 drugs and risk of heart attack

A
  • COX 2 selective drugs will inhibit the production of enzymes that promote vasodilation and inhibit platelet-induced occlusion
  • Clot formation can more easily occur
32
Q

Acetaminophen

A
  • Analgesic, fever reducer (similar to aspirin)
  • NO anti-inflammatory or anticoagulant effects
  • No GI tract irritation
  • first line drug for pain reduction (OA)
33
Q

Adverse effects of Acetaminophen

A
  • No GI effects, but can cause liver issues (liver necrosis)
  • can bind and inactivate liver proteins
  • produce oxidative stress, mitochondrial dysfunction that triggers liver tissue destruction
34
Q

Duloxetine (Cymbalta)

A

*Only FDA approved antidepressant for neuropathic pain

  • SNRI
  • Depression
  • Anxiety
  • often prescribed by pain physicians
35
Q
A

Medical Screening II (9 decks)

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